Hypothyroidism as a Response to EMF-Induced Chronic Inflammation (Part 1)

how thyroid hormone-producing cells initiate a self-destruct program in response to chronic inflammation (pyroptosis)

I wondered if there might be a slow modern-day killer of the thyroid gland that can affect us all. As the title reveals, my scientific inquiry led me to EMFs.

I won’t be focusing on dietary iodine deficiency here as a cause of hypothyroidism because this is no longer a likely factor in the developed countries. In fact, taking large amounts of iodine supplement for thyroid health (or other purposes) might be dangerous, given that most iodine supplements contain plenty of its ionic form - iodide. And excess iodide is used to precipitate the onset of autoimmune thyroiditis in research animals with a specific immunogenetic background (ref).

We need to start looking beyond iodine and beyond even selenium, magnesium, and vitamin D. While all these nutrients are important for health, we are now dealing with quite a different set of health challenges that have little to do with outright nutritional deficiencies. Low levels of these and other vitamins in the body may stem not from their low dietary intake but rather from how the body utilizes and depletes these nutrients when in constant state of inflammation. This concerns the thyroid health problem, too.

To underscore the immensity of the thyroid health problem, I’ll point out an alarmingly high prevalence of the hypothyroid condition in the US. According to a 2022 study: “an increasing percentage of the United States population is affected with hypothyroidism, with rates increasing from 9.5% in 2012 to 11.7% in 2019” (ref). And this could just be the tip of the iceberg. Clinical hypothyroidism is preceded by a subclinical form, which is likely more prevalent than clinical hypothyroidism but goes undiagnosed.

To understand how thyroiditis develops (thyroiditis is the inflammation and the eventual destruction of the thyroid gland), we need to look at several types of programmed cell death scenarios that can occur in the body: apoptosis, pyroptosis, and necroptosis. (I will leave out ferroptosis—cell death caused by too much iron.)

Apoptotis is the most physiologically benign and orderly type of cell death. It avoids the spillage of internal cellular contents and does not set off the cell danger response (CDR), nor does it activate the immune system. Cells that die off by apoptosis are fragmented and quietly engulfed and digested by macrophages or other scavenger cells. Unless it is massive due to an abnormal amount of apoptotic triggers, this type of programmed cell death maintains the homeostatic tissue turnover.

Pyroptosis, on the other hand, is cell death in response to inflammation. This type of the cell death program can be activated only in cells that contain structures called the inflammasomes, and thyroid follicle cells are among those that have it (ref). In addition to having the inflammasomes, thyroid follicle cells have a variety of external sensors called Toll-like Receptors (or TLRs) that can activate the inflammasomes. This activation doesn’t happen spontaneously but only when TLRs are themselves activated by damage-associated molecular pattern molecules, or DAMPs (ref). In the absence of DAMPs, there’s no TLR activation, no triggering of the inflammasomes, and no pyroptosis of the thyroid follicle cells. Your thyroid is safe, healthy, and productive.

So, where do DAMPs come from? DAMPs are proteins that normally stay inside the cell. They are spilled out when cells undergo necroptosis. This is another type of cell death program, which is induced by a molecule called TNF-alpha.

TNF-alpha is a pro-inflammatory cytokine produced during infections and it is indispensable for innate immune defenses. Blocking it, with drugs like Humira, may leave you immunocompromised. But TNF-alpha is also induced by something other than infections.

This ‘something other than infections’ is cellphone radiation.

I found a number of studies showing that the exposure of poor lab rats to 900-MHz cellphone radiation induces TNF-alpha in their tissues, including testis (ref), pancreas (ref), and brain and kidneys (ref). It is likely that other tissues, not yet tested, also produce more TNF-alpha when exposed to cellphone radiation.

Now that we are moving toward a higher frequency spectrum of 5G, I guess the researchers will have to update all their EMF experiments. But I bet, the effect on the living tissues will be similar if not worse.

What happens next when TNF-alpha levels are chronically elevated in the human body?

The cells that have the TNF-alpha receptors (TNFRs) could be instructed by TNF-alpha to undergo necroptosis in the absence of any overriding instructions by other molecular players. A necroptotic cell releases DAMPs. And when DAMPs reach the thyroid gland, they signal through TLRs to activate the inflammasomes inside the thyroid follicle cells, which forces the cells to self-destruct by pyroptosis. With enough of thyroid cells destroyed that way, the thyroid output capacity gets lower, which leads to the upregulation of thyroid-stimulating hormone (TSH) by the pituitary gland to force more thyroid hormone production by the remaining thyroid cells. Elevated TSH is diagnosed as hypothyroidism.

But this is not all. The spillage of internal thyroid antigens following the pyroptotic cell death makes them accessible to the immune system in the context of inflammation. The immune system in some patients may start producing autoantibodies against thyroid peroxidase (TPO) and thyroglobulin (Tg), and this is diagnosed as an autoimmune condition - Hashimoto’s thyroiditis. In addition, the inflamed thyroid tissue attracts and retains lymphocytes, which is also a symptom of Hashimoto’s. This secondary engagement of the immune system by an already inflamed and dying thyroid gland will keep contributing to the thyroid damage, although the immune system had nothing to do with initiating it. So don’t blame the immune system for what EMFs did.

It feels like this EMF-induced sequence of cellular events could eventually lead to thyroiditis in practically everyone. Yet surely not everyone in the modern world will develop thyroiditis and some people even recover from it. What’s rescuing their thyroid?

I will answer this question in Part II. Stay tuned.